Studies with three carcinogen-induced rat sarcomas showed that the threshold for tumor takes, growth characteristics, metastasis and hematologic changes produced by these tumors varied with implantation into different sites. With SQ and IM injections, 10 to the 5th power to 10 to the 4th power cells consistently yield tumors which grew as encapsulated locally invasive masses causing lung metastases in 8% of the hosts without altering blood coagulation. Identical injections beneath the renal capsule induced multinodular tumors which infiltrated the kidney and caused pulmonary metastases in 90% of the recipients. Intravascular thrombosis with these sarcomas caused diffuse necrosis and hemorrhage into the peritoneal cavity with death of the host from hypovolemic shock at four weeks. Blood from these rats exhibited fragmented and immature erythrocytes, thrombocytopenia, fibrinogen levels of zero and elevated titers of fibrin split products which were diagnostic of a consumptive coagulopathy. Subcapsular injections with single sarcoma cells yielded tumor takes in 38 of 50 rats, and these tumors slowly enlarged to weights of 50 to 70 grams, causing death of the host at 10 and 12 weeks from the same mechanisms described above. Similar injections with two of 40 cells produced discrete tumor colonies on the renal surface at 14 days, and the total number of tumor foci present on each kidney exhibited a near 1:1 correlation with the quantity of cells administered. Identical studies using immunized and allogenic recipients showed that injections with 10 to the 5th power to 10 to the 4th power cells produced multinodular tumor masses while challenges with 10 to the 3rd power to 10 to the 2nd power cells yielded takes originating from one to three discrete foci in each kidney. These results suggest that this tumor model may be useful in studing the clonal evolution of solid tumors in vivo and defining how stem line heterogeneity contributes to tumors growth in resistant hosts.